At a gross level, telomere ends resemble the ends of a double-strand break caused by DNA damage, yet telomeres do not activate the DNA damage response. An insight is offered as to how this response is suppressed. Two telomere-binding proteins, TRF2 and POT1, inhibit the activities of two upstream 'sensor' damage-responsive kinases, ATM and ATR, respectively. As these kinases initiate the signalling cascades that provoke the repair of damaged DNA, their inhibition by TRF2 and POT1 makes the telomere ends 'invisible' to the DNA repair machinery.
- Eros Lazzerini Denchi
- Titia de Lange